Essay on Cancer: Types, Development and Characteristics!
Contents:
- Essay on the Types of Cancer
- Essay on Development of Cancer
- Essay on the Characteristics of Cancer Cells
- Essay on Causes of Cancer
- Essay on Oncogenes and Cancer
Essay # 1. Types of Cancer:
There are more than a hundred distinct types of cancer according to their cellular origin, behaviour and response to treatment. However, to understand the cancer pathology, the distinction between benign and malignant tumors must be known.
A tumor or neoplasia (‘new growth’) is any abnormal and uncoordinated proliferation of cells, which may be either benign or malignant. A benign tumor do not grow indefinitely as their cells do not completely lose control over the rate of division, and remains usually covered by another epithelium confined to its original location, neither invading the surrounding normal tissues nor spreading to distant body sites.
A malignant tumor, on the other hand is capable of both invading the surrounding normal tissues and spreading throughout the body via the circulatory and lymphatic systems. Sometimes, cancer cells detach from the primary tumor and settle elsewhere in the body, where they grow and divide, and producing secondary tumors.
This process is called metastasis. Only malignant tumors are properly referred to as cancers and the metastatic property makes cancer so dangerous.
Both benign and malignant tumors can be classified into three groups according to the types of cells from which they arise. These are carcinomas, sarcomas, and leukemia’s or lymphomas.
Carcinomas are malignancies of epithelial cells, like breast tumor, skin tumors etc. It includes about 90% of human cancers. Sarcomas are rare in human; these are solid tumors of connective tissues, such as muscle, bone, cartilage and fibrous tissues.
Leukemia’s and lymphomas account for about 8% of human malignancies, arising from blood-forming cells and from cells of the immune system, respectively. Tumors are further classified according to the tissue of origin, like lung or breast carcinoma, and the type of cells involved, e.g., fibro-sarcoma arising from fibroblasts.
Essay # 2. Development of Cancer:
A tumor always originates from a single cell. The original progenitor cell that gives rise to a tumor may not acquire all the characteristics of a cancer cell. On the contrary, the development of cancer is a multistep process in which cells gradually become malignant through a progressive series of alterations.
One important indication in favour of this multistep development of cancer is that most cancers develop late in life. It is suggested that most cancers develop as a consequence of multiple abnormalities, which accumulate over a period of many years.
At the cellular level, the first step in the process of cancer development is tumor initiation which is thought to be the result of a genetic alteration leading to abnormal proliferation of a single cell. Cell proliferation then leads to the outgrowth of a population of clonally derived tumor cells.
Tumor progression then continues as additional mutations occur within cells of that tumor population. Some of these mutations confer some advantages like rapid growth, survival, invasion or metastasis to the cells of the tumor.
The descendants of these mutant cells will consequently become dominant within the tumor population. This process is called clonal selection, because a new clone of tumor cells has evolved on the basis of its mutant characters that confer a selective advantage.
Clonal selection continues throughout tumor development, so the tumors continuously become more rapid-growing and simultaneously the cells invade blood and lymphatic vessels allowing them to metastasize throughout the body (Fig. 3.38 and 3.39).
Essay # 3. Characteristics of Cancer Cells:
Cancer cells are commonly called as T- cells (transformed) in contrast to normal cells (N-cell).
A T-cell has three common and important characteristics:
(i) Hyperplasia:
Uncontrolled proliferation,
(ii) Anaplasia:
Structural abnormality and biochemical difference, and
(iii) Metastasis to detach from the point of origin and establish a new tumor at another site within the host body. An elaborated observation of cancer cells revealed following morphological, chromosomal and biological abnormalities.
Essay # 4. Causes of Cancer:
Carcinogen:
Several natural and artificial agents increase the frequency with which cells become cancerous are known as carcinogens. Many agents like radiation, chemicals and viruses have been found to induce cancer in both experimental animals and humans. Since malignancy is a complex and multistep process, many factors, however, may affect the development of same cancer.
Radiation and many chemical carcinogens act by damaging DNA and thus induce mutations which are thought to be the initial events leading to cancer development. These carcinogens are referred to as initiating agents. On the other hand, carcinogens that cause cancer by stimulating cell proliferation are referred to as tumor pro-motors. Phorbol ester and hormones particularly estrogens are important tumor pro-motors.
Types of Carcinogens:
Chemical carcinogens:
Two major groups of chemical carcinogens are recognized:
i. Direct Carcinogens:
Alkylating agents such as nitrogen mustard, EMS or ethyl-methanesulfonate and BPL or Beta- propiolactone are direct carcinogens. They directly act on cellular DNA to affect its structure so that cancer develops. These substances add alkyl groups or ethyl or methyl groups to guanine of DNA. Such alkylated DNA strands often get cross-linked.
ii. Indirect Carcinogens:
Most of the chemical carcinogens are indirect carcinogens. Initially, these compounds are found in a pro-carcinogen state. Pro-carcinogens, upon entry into the body, undergo metabolic activation to form the final or ultimate carcinogen which causes cancer.
Metabolic activation occurs in more than one step and the intermediate compounds formed during conversion of the pro-carcinogens into the ultimate carcinogen are called proximate carcinogens. For example, 2-acetylaminofluorane is a pro-carcinogen. It undergoes activation to produce the ultimate carcinogen called sulfate ester or N-hydroxyacetylaminofluorene.
Functionally, ultimate carcinogens are called as strong electrophiles or electron-deficient compounds having strong affinity for electron-rich groups of DNA and other macromolecules. These carcinogens bind covalently with purine, pyrimidine and phosphodiester groups in DNA to produce several mutations in DNA, which bring about malignant changes of the cells.
Examples of some Chemical Carcinogens:
Polycyclic aromatic hydrocarbons like benzopyrene, methylcholanthrene; aromatic amines like N-methyl-l-amino-azo benzene; alkylating drugs like cyclophosphamide and nitrogen mustard; natural toxin like aflatoxin of the fungus Aspergillus flavus — all these act as chemical carcinogens. Besides, some inorganic substances like asbestos, arsenic and cadmium chloride may show carcinogenic effects.
All chemical carcinogens are mutagens but all mutagens may not be carcinogenic in action. Both carcinogens and mutagens act on cellular DNA and induce chemical changes of DNA, but the chemical changes caused by carcinogen lead to uncontrolled proliferation of the affected cells. For example, formaldehyde and 5-bromouracil are mutagens but not carcinogenic, whereas benzopyrene, methylcholanthrene are carcinogens.
Physical Carcinogens:
i. Radiation:
Radiation from the sun (UV rays), cellular phones, radioactive radon gas, electric power lines, some household appliances, ionizing radiation emitted from X-ray machines, atomic bombs, decay of some radioactive materials and radon gas cause about 2 percent of all cancer death.
UV rays cause dimerization of thymine in DNA strand that leads to serious hamper in DNA replication and may produce breaks and cross linking of DNA strands that may have a carcinogenic consequence, especially for the skin. Ionizing radiations like X-rays and Gamma rays induce production of per-hydroxyl and superoxide radicals that act on DNA and produce breaks and cross-linking of DNA strands.
ii. Hormone-dependent Cancers:
An increase in the level of certain hormones in the body may stimulate the development of certain cancers in a particular sex. For instance, high estrogen may be correlated with high risk of breast and uterine cancers in females. Again, prostate carcinoma in males has been found to be associated with high androgen titre.
iii. Viruses:
In addition to above mentioned agents, some viruses are capable of infecting vertebrate cells, transforming them into cancer cells. These viruses are broadly classified into two groups depending on the presence of nucleic acid found within the mature virus particles — DNA tumor virus and RNA tumor viruses. (For detail see oncogenes given below).
Essay # 5. Oncogenes and Cancer:
Genes whose products may cause malignant transformation of eukaryotic cells are called oncogenes. Oncogenes may be cellular as well as viral genes.
i. Cellular Oncogenes:
The normal vertebrate genome contains several genes that may cause cancer upon activation. These genes are called C-oncogenes. Normally they remain inactive or in a proto-oncogene state.
C-oncogenes are found to be of four kinds:
(i) Class I oncogenes, when active, produce modified growth factors that cause uncontrolled cell division e.g., sis oncogene in monkeys produces an abnormal platelet- dependent growth factor (PDGF) which causes cancer of mesenchymal cells (Sarcoma)
(ii) Class II oncogenes, when active, produce modified membrane receptors and cells with such modified receptors can continually proliferate even in absence of growth factors, e.g., neuoncogenes of man produces modified membrane receptors for epidermal growth factor and it causes cancer of neuro-blasts
(iii) Class III oncogenes, when active, produce modified protein kinases which cause phosphorylation of various cellular proteins and increase their activities to such an extent that cells proliferate without any pause, e.g., abl oncogene concerned with chronic myeloid leukemia of man
(iv) Class IV oncogenes, when active; produce modified transcription factors, which leads to production of different unusual proteins and uncontrolled proliferation of cells, e.g., myc oncogene concerned with Burkitt’s lymphoma of man.
Proto-oncogenes normally remain inactive, but they get activated in different ways. Mutation, integration of retroviral genome at the vicinity of a proto-oncogene may act as a promoter or enhancer of transcription of the proto-oncogene, which thus, may convert into an active oncogene.
Moreover, translocation of a proto-oncogene from its original location to a different chromosomal location may activate the proto-oncogene to an active oncogene.
ii. Viral-oncogenes:
Both DNA and RNA viruses may contain oncogenes and they are called as oncogenic viruses:
(a) DNA Viral Oncogenes:
SV-40 (a simian virus), polyoma virus (a murine virus), adenoviruses (of different vertebrates), Epstein Barr virus (EB virus) causing human Burkitt’s lymphoma have circular double-stranded DNA with two sets of genes — early genes and late genes; only the early genes are oncogenes.
In permissive cells, the DNA virus goes through a lytic cycle and does not produce cancer. In non-permissive cells, the DNA virus produces cancer and does not go through any lytic cycle. The viral DNA upon entry into host cell is called as provirus and the provirus gets integrated into the host cell chromosome.
The ‘early gene’ of viral DNA produces T-anti- gens or tumor antigens but the Tate genes’ of viral DNA remain inactive. SV-40 DNA produces three T-antigens – large T, middle T and small t. The T antigens act like catabolic activator proteins or CAP which bind with cyclic- AMP to form CAP-cAMP complex.
This complex binds to host cell DNA and causes transcription of many genes which were so far inactive. Formation of new proteins leads to uncontrolled proliferation of cells.
(b) RNA Viral Oncogenes:
Cancer causing RNA viruses are called retroviruses, e.g., Rous sarcoma virus of chick and Rouscher’s leukemia virus. Retroviruses are thought to have acquired oncogenes from eukaryotic cells only.
Rous sarcoma virus has four genes:
(i) Gag coding for a viral antigenic protein,
(ii) Pol coding for reverse transcriptase enzyme,
(iii) Env coding for viral capsid protein and
(iv) Src coding for protein kinase.
After the viral RNA enters into host cell, it is transcribed into a DNA strand by reverse transcriptase. This complementary DNA strand now forms a double stranded DNA with reverse transcriptase. The DNA soon become circular and is called as provirus, which get integrated into host cell chromosome.
The viral genes produce their respective products and the src-product causes cancer. However, some progeny viruses may be produced, they do not cause rupture of the host cell but get attached to host cell-membrane and slowly get detached to infect other cells.
Cancers of Viral origin:
Till now six types of human cancers have been known to be caused by viruses. Cancers caused by DNA viruses include uterine cervix cancer by Papavo virus, hepatic cancer by hepatitis B virus (it may be caused by carcinogenic chemicals also), Burkitt’s lymphoma and nasopharyngeal cancer are caused by Epstein-Barr virus.
Cancers caused by RNA viruses include T-cell leukemia by HTLV or human T-cell leukemia virus and Kaposi’s sarcoma or cancer of blood vessel wall is caused by HIV or human immunodeficiency virus which also causes AIDS or acquired immunodeficiency syndrome.